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Effects of High Fat Diet Induced Obesity on Mitochondrial Biogenesis and Function – Impact of Exercise or Nicotinamide Mononucleotide (NMN)
Author(s) -
Uddin Golam Mezbah,
Yongson Neil,
Sinclair David,
Morris Margaret
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.777.8
Subject(s) - nicotinamide mononucleotide , nicotinamide adenine dinucleotide , endocrinology , medicine , mitochondrial biogenesis , nad+ kinase , nicotinamide , chemistry , citrate synthase , physical exercise , mitochondrion , biochemistry , enzyme
Exercise has known beneficial impacts on the metabolic outcomes of obesity. Exercise improves metabolism by up‐regulating mitochondrial activity, through increased levels of nicotinamide adenine dinucleotide (NAD + ). Recent studies suggest that the NAD + precursor nicotinamide mononucleotide (NMN) acts as an exercise mimetic by increasing NAD + levels. Here we compared the effects of exercise and NMN on the metabolic consequences of high‐fat diet (HFD) induced obesity. Sixty female C57BL6/J 5 week old mice were allocated across 5 interventions: Chow sedentary: CS; Chow exercise: CEX; HFD sedentary: HS; HFD NMN: HNMN; HFD exercise: HEX (12/group). After 6 weeks of diet exercise groups underwent treadmill exercise (15m/min for 45 minutes), 6 days per week for 6 weeks. NMN (500mg/kg body weight) was injected (IP) every day for the last 17 days. No significant alteration in body weight was observed in response to exercise or NMN. HEX and HNMN mice both showed significantly improved glucose tolerance compared to the HS group. Mitochondrial copy number was increased by NMN treatment (HNMN vs HS) but not by exercise. However, exercise, but not NMN, significantly ameliorated the HFD‐induced reduction in muscle citrate synthase activity. All HFD groups showed reduced PGC1 protein. Overall these data suggest that exercise and NMN improve glucose tolerance through different mechanisms involving mitochondria in a HFD induced obese mouse model.